The present invention relates generally to implantable medical devices, and more particularly to an implantable interventional device which is adapted to deliver electric impulse or shock therapies to the patient's heart upon detection of a ventricular tachycardia (VT) or ventricular fibrillation (VF), and to improvements in apparatus and methods for detecting and distinguishing pathologic tachycardias from physiologic tachycardias and for establishing the timing of the delivery of the appropriate therapy upon detection of pathologic VT or VF.
Sinus heart rates in normal healthy adults typically range upward to 160 beats per minute (bpm) during physical activity or exercise, emotional stress or excitement, or under the influence of various drugs including alcohol, caffeine or nicotine. Even higher rates, to 200 bpm may be experienced during strenuous exercise. Rates exceeding 100 bpm in these and similar circumstances are physiologic tachycardias. The heart rate of an individual with a normal healthy cardiovascular system will gradually, perhaps even quickly, decrease toward his or her customary resting rate when the factors leading to the increased rate have ceased.
In contrast, pathologic tachycardias are abnormal, arising from cardiovascular disease or disorders, and require medical treatment and appropriate therapy. A pathologic tachycardia occurring in the atrial chamber is usually hemodynamically tolerated because the excitable A-V junction tissue (between the atrium and ventricle) has a longer refractory period and slower conductivity than myocardial tissue. Hence, the rapid atrial contractions during atrial tachycardia typically will not induce correspondingly rapid ventricular contractions, but rather a ventricular rate of one-half or even one-third in the A-V conduction. Cardiac output remains relatively strong with a ventricular rhythm within or close to sinus rate.
However, pathologic tachycardia in the ventricles, the main pumping chambers of the heart, is not well tolerated because of the diminished cardiac output attributable to only partial filling of the chambers with oxygenated blood between the rapid contractions. Moreover, ventricular tachycardia (VT) tends to accelerate spontaneously to ventricular fibrillation (VF), in which the myocardial contractions become random and uncoordinated. Unlike atrial fibrillation, which is generally not life-threatening because of the relatively small percentage of cardiac output contributed by the atria, VF is characterized by the loss of synchronous contractions of the tissue in the main pumping chambers. The resulting drop in cardiac output will lead to death in minutes unless adequate cardiac output is restored within that interval.
Atrial tachycardia is relatively common, but patients who are symptomatic or at high risk may be treated with drugs, antitachycardia pacemakers, or in some extreme cases, including patients who suffer from atrial fibrillation, by performing a surgical A-V block and a ventricular pacemaker implant. The antitachycardia pacemakers, also used in patients who suffer VT, generally operate on the principle of overstimulating the heart (at a programmed rapid rate or variable rates) to suppress the ectopic activity that leads to premature atrial or ventricular contractions. Only pulses of relatively low energy content may be required to provide the desired stimulation. Interestingly, previous techniques used for terminating atrial flutter include high rate pacing of the atrium exceeding the flutter rate in an attempt to trigger atrial fibrillation, and spontaneous rapid reversion to normal sinus rhythm. In a technique sometimes referred to as cardioversion, tachycardia is broken by delivering higher energy electrical shocks to the heart. Unfortunately, antitachycardia and cardioversion therapies used for terminating VT can cause acceleration into VF.
Defibrillators are employed to apply one or more high energy electrical shocks to the heart to overwhelm the uncoordinated contractions of the various sections of the myocardial tissue and reestablish organized spreading of action potentials from cell to cell, and thereby restore synchronized contractions of the ventricles. Automatic implantable defibrillators were described in the literature at least as early as 1970, in separate articles of M. Mirowski et al. and J. Schuder et al. Steady innovations proposed since that time have included automatic implantable defibrillators which perform multiple functions of antitachycardia, cardioversion and defibrillation, and where appropriate, demand bradycardia pacing. In general, the desire is to use one or more pulse sequence or low level shock therapies for breaking VT before it spontaneously accelerates into VF, and, if that fails or if VF occurs without preliminary pathologic tachycardia, to resort to a high energy defibrillating shock.
The shocks, both lower energy for antitachycardia and high energy for defibrillation, are typically delivered from one or more output storage capacitors in the implanted device which are of sufficient size to store the electrical charge necessary for these functions. Energy requirements generally range from as little as 0.05 joule to up to 10 joules for cardioversion, and from 5 joules to about 40 joules for defibrillation, depending on the patient, the nature of the electrical waveform applied, and the efficiency of the energy transfer through the electrodes and into the heart tissue. It is imperative, particularly where VF is occurring, that the required energy be available at the time the shock is to be delivered. Multiphasic shocks have been found effective, and in any event, it is customary to provide a preset delay between successive shocks, and to inhibit further shocks when return to normal rhythm is detected.
As used in this specification, the terminology "shock" or "shocks" may include any pulse-type waveform, whether single phase or multiphase, which is delivered as antitachycardia, cardioverting or defibrillating therapy to a patient's heart in an effort to break, interrupt or terminate pathologic tachycardia or fibrillation and return the pumping action of the heart to a rate in the normal range; and "interventional device" includes any antitachycardia pacemaker, cardioverter, defibrillator or other device or combination thereof which is adapted to be implanted or otherwise worn by a human or animal subject for the purpose of intervening to deliver shocks to the heart in response to detection of an abnormally rapid heart rate. The waveform is not limited to any particular energy content or range of energy content, and indeed, the therapy may include burst stimulation or other conventional techniques for applying stimulation pulses (such as for rapid pacing) to break a VT.
The operation of implantable antitachycardia pacemakers, cardioverters, defibrillators and similar medical devices raises problems concerning the timing of delivery of the therapy, such as the timing of charging and firing of shock-producing output capacitors. In the first instance, it is necessary to distinguish between physiologic tachycardia and pathologic tachycardia to assure that the capacitors are not needlessly charged either frown states of full or partial depletion (discharge), and in the second instance, to guard against premature firing and discharge into the heart. U.S. Pat. No. 4,114,628 discloses an implantable device which automatically applies a defibrillating impulse to the patient's heart only when a predetermined time interval passes without cardiac activity. More elaborate detection schemes have been suggested. For example, in U.S. Pat. No. 3,805,795, the defibrillating shock is delivered upon detection of an absence of both electrical and mechanical physiological functions for a predetermined time interval.
In general, the prior art devices detect ECG changes and/or absence of a mechanical function such as rhythmic contractions, pulsatile arterial pressure, or respiration, and, in response, deliver the appropriate fixed or programmable therapy. Various types of additional sensors have been used for the latter functions, including pressure sensors in the heart, impedance measurements in the heart, flow probes in the aorta, flow probes in the pulmonary tract, and other extra-pacemaker or extra-defibrillator sensors. These sensors have not proved to be fully accurate or reliable.
It is a principal object of the present invention to provide improved techniques for treating ventricular tachycardia and/or fibrillation, including improved techniques for detecting tachycardia and distinguishing the normal physiologic type from the abnormal pathologic type.
A related object is the use, for such techniques, of a sensor which may be housed in the implanted interventional device itself or separately implanted, to detect position, change of position, and physical activity (or lack thereof) of the patient, and which applies an algorithm to reinforce or confirm (or contest or rebut) the ECG criteria, to improve the reliability of the decision regarding the propriety and timing of the intervention therapy available from the device.